In This Issue
Journal: Cancer Discovery (2022)

In This Issue| June 02 2022 In This Issue Author & Article Information Online Issn: 2159-8290 Print Issn: 2159-8274 ©2022 American Association for Cancer Research.2022American Association for Cancer Research. Cancer Discov (2022) 12 (6): 1397–1399. https://doi.org/10.1158/2159-8290.CD-12-6-ITI Related Content A commentary has been published: Characterization of INCB086550: A Potent and Novel Small-Molecule PD-L1 Inhibitor A commentary has been published: Identification of Functional Heterogeneity of Carcinoma-Associated Fibroblasts with Distinct IL6-Mediated Therapy Resistance in Pancreatic Cancer A commentary has been published: Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML View more A commentary has been published: Integrated Multiomic Profiling Identifies the Epigenetic Regulator PRC2 as a Therapeutic Target to Counteract Leukemia Immune Escape and Relapse A commentary has been published: The Spatial Landscape of Progression and Immunoediting in Primary Melanoma at Single-Cell Resolution A commentary has been published: Precision Combination Therapies Based on Recurrent Oncogenic Coalterations A commentary has been published: PD-1 Blockade in Solid Tumors with Defects in Polymerase Epsilon A commentary has been published: Reverse Transcriptase Inhibition Disrupts Repeat Element Life Cycle in Colorectal Cancer A commentary has been published: Discovery, Preclinical Characterization, and Early Clinical Activity of JDQ443, a Structurally Novel, Potent, and Selective Covalent Oral Inhibitor of KRASG12C View less Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record June 2 2022 Citation In This Issue. Cancer Discov 1 June 2022; 12 (6): 1397–1399. https://doi.org/10.1158/2159-8290.CD-12-6-ITI Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search Proofreading defects produced from mutations in the DNA polymerase epsilon (POLE) gene contribute to a hypermutated genome that can potentially sensitize tumors to immune checkpoint blockade. Despite this, many POLE-mutant tumors do not demonstrate a robust response to this type of therapy. Rousseau and colleagues conducted a multicenter clinical trial in patients with POLE-mutated solid tumors and showed that only mutations in the DNA binding or catalytic site of the exonuclease domain of POLE contributed to high tumor burden and subsequent increases to T-cell infiltration and response rates to anti–PD-1 therapy, suggesting their use as a biomarker of anti–PD-1 response. See article, p. 1435. Escape from the “graft-versus-tumor” effect represents the main driver of leukemia relapses after allogeneic hematopoietic cell transplantation. In up to 40% of cases, the expression of HLA class II molecules is lost from the surface of leukemic cells, without evidence of... You do not currently have access to this content.